Assistant Professor of Internal Medicine
- Cardiovascular Medicine
PhD, University of Toronto, Canada
MD, University of Toronto, Canada
Residency, New York Presbyterian Hospital/Memorial Sloan-Kettering Cancer Center/Weill Cornell Medical Center, New York
Fellowship, Research, Howard Hughes Medical Institute Children's Hospital, Harvard Medical School, Boston
Fellowship, Cardiology, Brigham & Women's Hospital/Harvard Medical School, Boston
Obesity, diabetes and metabolic syndrome are major public health problems and significant risk factors for heart disease in the United States and world-wide. As a clinical cardiologist, I am faced with managing these conditions in patients on a regular basis. My lab is currently focused on studying ion channels as regulators of cellular metabolism in skeletal muscle, adipose tissue and myocardium. Specifically, my research interests focus on intracellular signaling of transient receptor potential channels (including TRPV3, TRPV4 and TRPM7), and the recently identified volume regulatory anion channel SWELL1 (LRRC8a) as they relate to obesity and metabolism. To do this we combine cellular electrophysiology, calcium imaging (GCaMP6) and novel genetic techniques (including transient and stable lenti/AAV-shRNA-mediated knockdown and CRISPR/cas9-mediated knockout) in cultured cells (mouse and human) and freshly isolated primary cells (adipocytes, skeletal muscle fibers, cardiomyocytes). Genetic loss-of-function (CRISPR/cas9-mediated and conventional) mouse models for these ion channels are also used to examine the contributions of these ion channels in vivo and in disease settings. Through a close collaboration with the bariatric surgery program we also have access to freshly isolated human adipocytes from obese and lean patients for acute electrophysiological experiments and long-term culture.
Van den Boogert M,
Ion channel-kinase TRPM7 is required for maintaining cardiac automaticity.
Proc Natl Acad Sci USA.
Van den Boogert M,
Timing of myocardial trpm7 deletion during cardiogenesis variably disrupts adult ventricular function, conduction, and repolarization.
TRPV4 is a regulator of adipose oxidative metabolism, inflammation, and energy homeostasis.
Date Last Modified: 05/20/2015 -